A 68-year-old diabetic female on dialysis presented with a chronic right heel ulcer (3.4 cm X 3.1 cm) of greater than 3 months duration. Photograph of the wound after thorough wound bed preparation over the course of 2 weeks.

Neuropathic arthropathy (or neuropathic osteoarthropathy), also known as Charcot joint (often "Charcot foot"), refers to progressive degeneration of a weight bearingjoint, a process marked by bony destruction, bone resorption, and eventual deformity. Onset is usually insidious.

If this pathological process continues unchecked, it could result in joint deformity, ulceration and/or superinfection, loss of function, and in the worst-case scenario, amputation or death. Early identification of joint changes is the best way to limit morbidity.

Diabetes mellitusneuropathy (the most common in the U.S. today, resulting in destruction of foot and ankle joints), with Charcot joints in 1/600-700 diabetics. Related to long-term poor glucose control.

Neurotrauma: Loss of peripheral sensation and proprioception leads to repetitive microtrauma to the joint in question; this damage goes unnoticed by the neuropathic patient, and the resultant inflammatory resorption of traumatized bone renders that region weak and susceptible to further trauma. In addition, poor fine motor control generates unnatural pressure on certain joints, leading to additional microtrauma.

Diabetes is the foremost cause in America today for neuropathic joint disease,[1] and the foot is the most affected region. In those with foot deformity, approximately 60% are in the tarsometatarsal joints (medial joints affected more than lateral), 30% Metatarsophalangeal joints and 10% have ankle disease. Over half of diabetic patients with neuropathic joints can recall some kind of precipitating trauma, usually minor.

Patients with neurosyphilis tend to have knee involvement, and patients with syringomyelia of the spinal cord may demonstrate shoulder deformity.

Oblique view X-ray in a 45-year-old male diabetic revealed a divergent, Lisfrancdislocation of the first metatarsal with associated lesser metatarsal fractures.

The same 45-year-old man with diabetes mellitus presented with a diffusely swollen, warm and non-tender left foot due to Charcot arthropathy. There are no changes to the skin itself.

The clinical presentation varies depending on the stage of the disease from mild swelling to severe swelling and moderate deformity. Inflammation, erythema, pain and increased skin temperature (3–7 degrees Celsius) around the joint may be noticeable on examination. X-rays may reveal bone resorption and degenerative changes in the joint. These findings in the presence of intact skin and loss of protective sensation are pathognomonic of acute Charcot arthropathy.

Roughly 75% of patients experience pain, but it is less than what would be expected based on the severity of the clinical and radiographic findings.

Clinical findings include erythema, edema and increased temperature in the affected joint. In neuropathic foot joints, plantar ulcers may be present. Note that it is often difficult to differentiate osteomyelitis from a Charcot joint, as they may have similar tagged WBC scan and MRI features (joint destruction, dislocation, edema). Definitive diagnosis may require bone or synovial biopsy.

First, it is important to recognize that two types of abnormality may be detected. One is termed atrophic, in which there is osteolysis of the distal metatarsals in the forefoot. The more common form of destruction is hypertrophic joint disease, characterized by acute peri-articular fracture and joint dislocation. According to Yochum and Rowe, the "6 D's" of hypertrophy are:

Distended joint

Density increase

Debris production

Dislocation

Disorganization

Destruction

The natural history of the joint destruction process has a classification scheme of its own, offered by Eichenholtz decades ago:

Stage 0: Clinically, there is joint edema, but radiographs are negative. Note that a bone scan may be positive before a radiograph is, making it a sensitive but not very specific modality.

Stage 2: Decreased local edema, with coalescence of fragments and absorption of fine bone debris

Stage 3: No local edema, with consolidation and remodeling (albeit deformed) of fracture fragments. The foot is now stable.

Destroyed Tarsometatarsal joints in the medial left foot, with fracture and dislocation of fragments; these are classic findings. Also note loss of the foot arch and acquired flat foot (pes planus) deformity.

Atrophic Features:

"Licked candy stick" appearance, commonly seen at the distal aspect of the metatarsals

Once the process is recognized, immobilization with a total contact cast will help ward off further joint destruction. Walking braces controlled by pneumatics are also used. Surgical correction of a joint is rarely successful in the long-term in these patients.

It can take 6–9 months for the edema and erythema of the affected joint to recede.

Outcomes vary depending on the location of the disease, the degree of damage to the joint, and whether surgical repair was necessary. Average healing times vary from 55–97 days depending on location. Up to 1–2 years may be required for complete healing.